ISCHAEMIC COLITIS. Dr. Philip Chan McMaster University

ISCHAEMIC COLITIS Dr. Philip Chan McMaster University What is Ischaemic Colitis Ischaemic colitis (IC) • Term first coined in 1966 by Martson et al....
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ISCHAEMIC COLITIS Dr. Philip Chan McMaster University

What is Ischaemic Colitis Ischaemic colitis (IC) • Term first coined in 1966 by Martson et al. to refer to a clinical entity with diverse causes but fundamentally characterized by circulatory insufficiency of the colon resulting in varying degrees of tissue necrosis

Spectrum of conditions: • reversible colopathy - transcient colitis chronic colitis - stricture - gangrene fulminant universal colitis

Why Should We Care? • Part of the broad spectrum of acute mesenteric ischaemia (AMI) • 1 of 1000 hospitalizations due to intestinal vasculopathy • IC most common form of intestinal ischaemia • Despite advances in understanding of pathophysiology, diagnosis, and Rx of AMI, mortality rates haven’t changed much over the past half-century • Unlike other forms of AMI, generally has good prognosis

Anatomy • Arterial supply to small and large bowel provided by: – superior mesenteric artery (SMA) – inferior mesenteric artery (IMA) – internal iliac arteries

• Collateral flow exists between the three systems

Anatomy cont’d

SMA

IMA

Internal iliac

Intestinal Ileocolic Right colic Middle colic

Jejunum and ileum Ileum, cecum, ascending colon Distal ascending colon, hepatic flexure Proximal transverse colon

Left colic Sigmoid Superior rectal

Distal transverse, splenic flexure Descending colon, sigmoid Proximal part of rectum

Middle rectal Inferior rectal

Midpart of rectum Distal rectum and anal canal

Collaterals • Splanchnic-Systemic collateral: – Superior rectal to inferior rectal

• Splanchnic-Splanchnic collaterals: – A series of arcades interconnect neighbouring branches of SMA; same occurs with IMA – Arcades of IMA and SMA interconnect near base (away from colon); called Arc of Riolan – Connection of arcades at border (near the colon) called marginal artery of Drummond

• Intramural collaterals: – Bowel contains a submucosal vascular network that can maintain viability of short segments during occlusion

Anatomic Variations – R and middle colic arteries missing, diminutive or have variable origins in 10-29% of pts – 5% of population have underdeveloped/absent connections in watershed region of splenic flexure (Griffith’s point) – marginal artery of Drummond poorly developed in R colon in 50% of population – rectosigmoid junction supplied by narrow terminal branches of IMA – Vasa recta in R colon fewer in number, origin occurs further from bowel wall – end vessels particularly sensitive to vasospasm

Areas of Vulnerability • Most vulnerable are watershed areas - the splenic flexure, ascending colon, and sigmorectal regions • Reeders et al.(1984) - Left side of colon and rectum affected 75% of time with 23% involving splenic flexure • More recent reports show increasing incidence of right colon involvement • May reflect increased incidence of non-occlusive ischaemia

Etiology • Occlusive vs. non-occlusive • Arterial vs. venous – Arterial - large vessel vs. small vessel • Large vessel - emboli, thrombi, atheromatous debris • Small vessel - vasculitides, DM, radiation

– Venous • hypercoagulable states, portal HTN, pancreatitis • extrinsic obstructions – a) outside bowel eg carcinoid, amyloidosis b) within bowel eg adhesions, volvulus, hernia

Etiology cont’d • Non occlusive – any low-flow states eg shock, CHF, sepsis – medications eg digoxin, OCP, diuretics, cocaine, pseudoephedrine, NSAIDs, alosetron – Prolonged/strenuous exercise

• Post-op – Most frequently after aortic reconstruction (incidence 0.3-10%) – difficult dx - diarrhea, incr. wbc, hypotension, incr. fluid requirements are clues

Pathophysiology • Multifactorial – ischemic tissue injury – systemic release of inflammatory cytokines due to endotoxemia and portal bacteremia 2º to increased mucosal permeability – reperfusion injury – MSOF

Clinical Presentation • No pathognomonic signs or symptoms • Typical patient - elderly, male, vasculopath, DM, renal insufficiency • Non specific symptoms (Longo et al, 1992): abdo pain (typically LLQ) - 87% diarrhea - 68% distension - 63% nausea/vomiting - 38% pain abrupt in onset, crampy, mild; steadily progressive

Clinical Presentation cont’d • Less common symptoms: – lower GI bleed -> moderately advanced injury – stricture formation

• Subset of younger patients: – predominately female, acute onset, rectal bleeding > abdo pain, lack of risk factors, generally self-limited

Clinical Presentation cont’d • Risk factors: – age > 50 – CHF – arrhythmias – recent MI – hypotension, sepsis, hypovolemia

Clinical Presentation cont’d • Signs: – tenderness – abdominal distension – low-grade fever – tachycardia – fecal occult blood – peritoneal signs

Patterns of presentation M ild

In te rm e d ia te

S evere

50

30

1 0 -2 0

L ayers in v o lv e d

o n ly m u c o s a & subm ucosa

S y m p to m s

a b d o p a in , b lo o d y d ia rrh e a C o n s e rv a tiv e

v a ria b le th ic k n e s s o f th e m u s c u la ris S im ila r to m ild

tra n s m u ra l g a n g re n o u s n e c ro s is p e rito n itis

V a ria b le

L a p a ro to m y

s tric tu re o r p e rs is te n t c o litis

H ig h m o rta lity

% of cases

T r e a tm e n t S e q u e la e

N o lo n g te rm s e q u e la e

Differential Diagnosis • Infectious colitis - stool C&S, C.diff, pseudomembranes on colonoscopy • Ulcerative colitis - younger age of pt, rectal involvement, longer duration of sx • Crohn’s colitis – terminal ileum involvement, fistulas, fissures on colonoscopy • Colon CA - slower onset of sx; colonoscopy • Diverticulitis - CT often useful • Toxic megacolon - massive colonic dilation • Pancreatitis

Investigations • Diagnosis mainly clinical - high index of suspicion! • Imaging and bloodwork adjunctive role • Definitive diagnosis most frequently obtained by endoscopy • Angiography rarely diagnostic

Imaging modalities • AXR – rarely diagnostic; useful in ruling out other pathology – non-specific findings eg distension – most characteristic findings - “Thumbprinting” due to submucosal edema and hemorrhage – multiple, round, smooth, soft tissue densities projecting into air-filled colonic lumen – worrisome signs - pneumatosis intestinalis, portal venous air, free air - are rarely seen and assoc. with advanced ischaemia

Imaging Modalities cont’d • CT – similar to AXR in that findings usually non-specific – may be normal in pts with early infarction and may be abnormal in only 1/3 of pts with established IC – most common findings - circumferential wall thickening due to edema or hemorrhage; luminal narrowing; polypoid filling defects (equivalent to “thumbprinting”)

Imaging modalities cont’d • MRI – not frequently used

• Angiography – not usually indicated; rarely diagnostic – often reveals patent major visceral vessels, likely since most vessel lesions causing IC are peripheral and there-fore difficult to detect

• Doppler U/S – highly specific for identifying occlusions/severe stenoses but doesn’t establish Dx b/c occlusion of splanchnic vessels can be present in asymptomatic pts.

Laboratory investigations • No sufficiently specific chemical/enzymatic markers – Leukocytosis with neutrophilia – Metabolic acidosis – Increased lactate or LDH – Elevated phosphate – Elevated CK – Elevated ALP

Endoscopy • Can yield definitive diagnosis and grading of disease severity – acute - pale mucosa with areas of petechial hemorrhage (mild ischemia) – progressively darker mucosa (dark blue to black) and sloughing/ulcerations signals more severe disease – may be difficult to distinguish based on visual appearance alone from other forms of colitis eg CD, UC, infectious, radiation

Endoscopy cont’d • Biopsy for histologic exam can be useful: – Crypt destruction – Sloughing of epithelial cells – Edema – Few inflammatory cells

• Doesn’t give info on depth of involvement

Intraoperative Monitoring • Prevention of IC after aortic surgery important b/c of high asso. mortality • Longo et al. (1996) - 54% mortality among those who develop IC after aortic surgery; 2/3 required colectomy (89% mortality) • Various monitoring modalities suggested: – Doppler US – IV fluoresein administration – Intramural pH measurement

• Zelenock et al (1989) – colonic and/or pelvic revascularization at time of reconstruction lessens risk of post-op IC

Management • For all patients: – NPO, fluid resuscitation, broad spectrum antibx (no clinical evidence of benefit; recommendations based on several old experimental studies) – correct conditions associated with/predisposing to IC eg correcting low flow states, stop offending meds – avoid narcotics initially – may blunt signs of peritonitis and promote abdo distension – cathartics contraindicated b/c of risk of perforation – these measures usually sufficient for those with mild IC

Indications for Surgery • Acute indications: – peritonitis – massive bleeding – universal fulminant colitis +/- toxic megacolon

• Subacute indications: – failure to respond to conservative measures – recurrent bouts of sepsis

• Chronic indications: – symptomatic colon stricture – symptomatic segmental ischaemic colitis

Prognosis • Mild to moderate disease - low mortality – Usually resolves within 2 wks – Followup necessary to r/o recurrent colitis or stricture

• Pts undergoing surgery have ~ 60% mortality • 20% develop chronic colitis • 5% experience recurrence

Chronic Ischaemia • More than 95% of cases of chronic mesenteric ischemia are due to atherosclerotic mesenteric arterial stenosis • uncommon, but not rare; may be underreported • female> male, age > 60, vasculopaths • classic symptomatic triad of postprandial pain, fear of eating (sitophobia), and involuntary weight loss occurs with advanced disease • most consistent symptom is postprandial pain beginning 15-30min after eating; due to incr. metabolic demands

Chronic Ischaemia • pain generally epigastric or periumbilical; dull, gnawing, or aching in quality; and crampy or colicky over time • With mild disease, small meals don’t induce abdo pain; with advanced/severe occlusion, pain more severe, longer lasting, constant, and is induced by smaller meals • On exam: – weight loss and malnutrition – abdo tenderness diffuse and mild, w/o rebound or guarding, even during an episode of severe pain – severity of the pain is out of proportion to the paucity of abdominal findings

Chronic Ischaemia • Diagnosis: – Must r/o other pathologies first – Angiography to confirm the diagnosis, to assess disease severity, and to plan revascularization – Angiographic findings of

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